to 5^th sick days of gastroenteritis, tending to occur repetitively[1]. The main findings are (1) healthy term infants with seizures between 4 to 6 days of life (2)Gastroenteritis symptoms were not observed in most cases (3) Rotavirus was detected only in stool specimens (4) no evidence of CSF pleocytosis (5) Characteristic diffusion-weighted imaging (DWI) pattern on MRI [8].

Figure 3. Schematic illustration of possible mechanisms by which rotavirus infection can cause central nervous system manifestation.

The following mechanisms have been proposed for Central nervous system manifestations following rotavirus infections (figure 3). First, CNS-driven symptoms such as vomiting, sickness, loss of appetite, and malaise are considered brain-gut communication in rotavirus infection. This includes activating the vagal nerves that project to regions of the brain via enterotoxin non-structural viral protein 4-dependent 5-hydroxy tryptamine release [9]. Second, previously described CNS complications are explained as direct CNS effects. Potential mechanisms include:(1) direct viral invasion into the CNS (2) CNS entry of deleterious brain-damaging mediators; and (3) CNS entry of activated circulating leukocytes [10]. The activation of brain microglia which release reactive oxygen and nitrogen species and cytokines which are toxic to the premyelinating oligodendrocytes is the principal initiating event in systemic infection/inflammation leading to White matter injury [11].The following mechanisms have been proposed for Central nervous system manifestations following rotavirus infections (figure 3). First, CNS-driven symptoms such as vomiting, sickness, loss of appetite, and malaise are considered brain-gut communication in rotavirus infection. This includes activating the vagal nerves that project to regions of the brain via enterotoxin non-structural viral protein 4-dependent 5-hydroxy tryptamine release [9]. Second, previously described CNS complications are explained as direct CNS